OBJECTIVE To conduct a systematic review of the available literature for primary research articles identifying potential gene mutations, polymorphisms and other molecular regulatory mechanisms related to trigeminal neuralgia in order to identify the genetic and molecular models of primary trigeminal neuralgia currently being investigated. METHODS PubMed and Web of Science were systematically searched to identify primary research articles discussing genetic predictors of trigeminal neuralgia and neuropathic pain that were published prior to July 2020. This review was conducted according to PRISMA guidelines. RESULTS Out of the 333 articles originally identified, a total of 14 papers were selected for study inclusion. These articles included 5 human studies, 6 mouse studies and 3 rat studies. Four articles investigated sodium channels, 1 investigated a sodium channel and nerve growth factor receptor, 2 investigated potassium channels, 1 investigated calcium channels, 1 investigated the downstream regulatory element antagonist modulator protein, 1 investigated the dynorphin-kappa opioid receptor system, 1 investigated TRPA1, 1 investigated the Nrg1/ErbB3/ErbB2 signaling complex, 1 investigated a serotonin transporter and 1 investigated potassium channels, sodium channels, calcium channels, chloride channels, TRP channels and gap junctions. CONCLUSION Researchers have identified multiple genetic and molecular targets involved with potential pathophysiologies that have a relationship to the creation of trigeminal neuralgia. At this time, there does not seem to be clear causal frontrunner, demonstrating the possibility that genetic predisposition to trigeminal neuralgia may involve multiple genes and/or downstream products, such as ion channels.

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三叉神经痛的分子机制：系统评价

目的 对现有的主要研究文章进行系统回顾，以确定与三叉神经痛相关的潜在基因突变、多态性和其他分子调控机制，以确定目前正在研究的原发性三叉神经痛的遗传和分子模型。方法 系统地搜索 PubMed 和 Web of Science，以确定 2020 年 7 月之前发表的讨论三叉神经痛和神经性疼痛的遗传预测因素的主要研究文章。本次审查是根据 PRISMA 指南进行的。结果 在最初确定的 333 篇文章中，共有 14 篇论文被选入研究。这些文章包括 5 项人体研究、6 项小鼠研究和 3 项大鼠研究。四篇文章研究了钠通道，1 项研究了钠通道和神经生长因子受体，2 项研究了钾通道，1 项研究了钙通道，1 项研究了下游调节元件拮抗剂调节蛋白，1 项研究了强啡肽-kappa 阿片受体系统，1 项研究了 TRPA1，1 项研究了 Nrg1/ ErbB3/ErbB2 信号复合体，1 项研究了血清素转运蛋白，1 项研究了钾通道、钠通道、钙通道、氯通道、TRP 通道和间隙连接。结论 研究人员已经确定了涉及潜在病理生理学的多个遗传和分子靶标，这些病理生理学与三叉神经痛的产生有关。这个时候，似乎没有明确的因果领跑者，